This page lists the Department of Physiology labs by principal investigator. Learn about the broader goals for study within the labs, as well as details on individual faculty labs and teams.
Focusing on neuron activity that processes vestibular sensory signals and on oculomotor and electromyographic recordings.
Jim Baker's interests are in systems neurophysiology and neuroanatomy. Dr. Baker’s laboratory focused on neuron activity that processes vestibular sensory signals and on oculomotor and electromyographic recordings. The laboratory is no longer active as of 2013. Dr. Baker maintains active collaborations with the laboratories of Drs. Disterhoft, Heckman, Miller, and others. His areas of expertise are neuron recordings from conscious animals, general neuroanatomy, and technical aspects of neuroscience experimentation across a wide range of approaches. Faculty, staff, and students in any area of neuroscience, especially systems neuroscience, are welcome to come to Jim Baker to discuss their ideas and technical situations.
For publication information and more, see James Baker, PhD, faculty profile.
Defining the principles underlying the normal and abnormal operation of the basal ganglia.
Our research focuses on the basal ganglia, a group of subcortical brain nuclei that are critical for voluntary movement, learning and motivation, and the primary site of dysfunction in psychomotor disorders such as Parkinson's disease, Huntington's disease, obsessive-compulsive disorder and addiction. Our objectives are to define the principles underlying the normal and abnormal operation of the basal ganglia. Our hope is that this information will provide the foundation for the rational development of therapies that more effectively treat the symptoms or underlying causes of these disorders.
We utilize multiple experimental approaches including electrophysiology, 2-photon imaging, anatomical and molecular profiling, and viral vector-based techniques including optogenetics, pharmacogenetics and knockdown of synaptic receptors and ion channels. Our research is supported by the National Institute for Neurological Disorders and Stroke and the Cure Huntington's Disease Initiative.
For publication information and more, see Mark D Bevan, PhD, faculty profile.
Understanding the cellular and molecular building blocks of basal ganglia macrocircuit.
To date, millions of people in the US suffer from neurodegenerative diseases. Current therapeutic strategies are limited, short-lived, and ineffective. Our research seeks to provide the mechanisms that underlie the pathogenesis of Alzheimer's Disease, Parkinson’s disease, and Huntington’s Disease. We hope to translate our insights into developing novel treatments for these neurological disorders.
Alzheimer's disease is the most common neurodegenerative disease and it is the most common underlying cause of dementia. It affects primarily the cortex and hippocampus. Severe synapse loss and inclusions can be observed. Our research seek to delineate the cellular processes that lead to the network dysfunction and the endogenous clearing mechanism of oligomers.
Parkinson’s disease and Huntington’s disease are the two major neurodegenerative diseases that affect the motor function. Our research interests center on better understanding the cellular and molecular building blocks that make up the basal ganglia macrocircuit as well as their implications in both health and disease.
An effective communication in the brain involves proper controls of how signals are generated, how they are terminated, and how they are spatiotemporally distributed. This process involves a complex architecture of ion channels, receptors, synapse, release and clearance machinery, etc. Our lab studies how this is achieved and how it is altered in disease conditions. The main focus is on intrinsic excitability, neurotransmission, and their regulation by astrocytes.
Using cell-population transcriptomic analysis as a guide, a more effective and targeted electrophysiological analyses can be devised. The combination cell-specific Cre-driver lines, Cre-responsive transgenic mice and viral constructs forms a very powerful research tool that will allow us to tackle difficult research question that would not be otherwise possible.
Our research is currently funded by the NINDS, NIA/CNADC, DoD, PDF, NMF, APDA, and CHDI
For publication information and more, see C Savio Chan, PhD, faculty profile.
Contact the Lab at 312-503-1146.
Seeking to understand the link between synaptic dysfunction and neuropsychiatric disorders and neurodevelopmental disorders.
Research in our laboratory is directed at understanding the mechanisms of synaptic transmission and plasticity, and the role that glutamate receptors have in brain function and pathology. We use a multidisciplinary approach including in vitro electrophysiological recording, optogenetics, cellular imaging, mouse behavior, and biochemical techniques. We ultimately seek to understand the link between synaptic dysfunction and neuropsychiatric disorders and neurodevelopmental disorders. Current projects are investigating altered synaptic signaling in mouse models of obsessive compulsive disorder, schizophrenia, and fragile X syndrome.
John Marshall (NUIN)
Yiwen Zhu (DGP)
We study the neurobiology of associative learning in the mammalian brain at the molecular, cellular and systems levels using both in vivo and in vitro techniques. Our laboratory focuses on characterizing how neurons store new information during associative learning. An important component of our research program is identifying mechanisms for altered learning in aging. We use a combination of behavioral, biophysical and molecular biological approaches to address these questions.
Eyeblink conditioning is our primary model paradigm to assess associative learning. This Pavlovian task offers excellent stimulus control, ease of precise behavioral measurement, robust associative learning, and can be used to test both human and non-human animal subjects. We study rabbits , rats, mice, or humans depending upon the question being asked. We also use a broad set of additional techniques, including fear conditioning, spatial navigation in the Morris water maze and others, to assess other types of behavior to evaluate the specificity of experimental manipulations on mechanisms of associative learning.
Our program focuses on characterizing the ways in which neurons store new information during associative learning at the cellular and subcellular levels. Experiments focus on the hippocampus, a paleocortical region involved in transferring information during learning from the short- to long-term memory store. We make biophysical measurements from hippocampal brain slices taken from eyeblink-trained animals to define what ionic mechanisms underlie the changes in neuronal excitability recorded in the intact animal. An important focus of our research is on cellular mechanisms for altered learning in aging. Recently, we have incorporated calcium-imaging techniques using both a charge-coupled device (CCD) camera system and a two-photon laser scanning microscopy (2P-LSM) system to investigate learning- and aging-related changes in calcium properties in CA1 pyramidal neurons.
Our laboratory conducts multiple-single neuron recording experiments using chronically implantable microdrives in rabbits as they perform eye blink conditioning, an associative memory task. We take advantage of an integrated approach combining several techniques such as paired recordings from anatomically identified neurons, optogenetic, immunohistochemistry, light and electron microscopy applied to wild-type and transgenic animals. We use these techniques to test hypotheses about the neurophysiological properties and the functional role of neurons from brain regions that are involved in associative memory such as the prefrontal cortex, hippocampus, thalamus, and the basal ganglia.
Magnetic resonance imaging permits examination of the entire brain simultaneously and observation of changes in brain activity in the same individual over time. Functional magnetic resonance imaging is being done in rabbits with our collaborators Daniel Procissi and Lei Wang.
Daniel Curlik, PhD
Dina Simkin, PhD
Natividad Ybarra, PhD
Investigating the mechanisms of motor output the spinal cord in both normal and disease states.
Neurons in the spinal cord provide the neural interface for sensation and movement. Our lab focuses on the mechanisms of motor output in both normal and disease states (spinal injury, amyotrophic lateral sclerosis). We use a broad range of techniques including intracellular recordings, array recordings of firing patterns, 2-photon imaging, pharmacological manipulations, and behavioral testing. These techniques are applied in in vitro and in vivo animal preparations. In addition we have extensive collaborations with colleagues who study motor output in human subjects.
For publication information and more, see Charles J Heckman, PhD, faculty profile.
Studying the distributed processing modules (DPMs) that link the basal ganglia and the cerebellum to different functional regions of the cerebral cortex.
The distributed processing modules (DPMs) that link the basal ganglia and the cerebellum to different functional regions of the cerebral cortex are the focus of current research activity in the Houk lab. This work is founded on motor systems neuroscience, a field in which we begin to understand integrated functions that combine cellular, molecular and circuit level mechanisms into actions which may represent essential operations of the brain. Such essential operations could then be used over and over by the modular networks of the brain in order to control (either separately or in combination) thinking, planning of action, and/or the generation of motor commands for implementing movement. A topic of particular interest is the distributed multifaceted learning that occurs throughout our lifetime and serves to shape our personality.
For publication information and more, see James C Houk, PhD, faculty profile.
- Houk JC (2012) Action selection and refinement in subcortial loops through basal ganglia and cerebellum. In: Modelling natural action selection (chapter 10), edited by Seth AK, Prescott TJ, and Bryson JJ, Cambridge University Press, Cambridge, pp. 176-207.
- Scheidt RA, Zimbelman JL, Salowitz NM, Suminski AJ, Mosier KM, Houk J, and Simo L (2012) Remembering forward: Neural correlates of memory and prediction in human motor adaptation. Neuroimage 59: 582-600.
- Keifer J and Houk JC (2011) Modeling signal transduction in classical conditioning with network motifs. Front. Mol. Neurosci. 4:9. doi: 10.3389/fnmol.2011.00009
- Hill, S. K., B. A. Griffin, J. C. Houk and J. A. Sweeney (2011). "Differential effects of paced and unpaced responding on delayed serial order recall in schizophrenia." Schizophrenia Research 131: 192-197.
- Houk, J. C. (2011). "Syntax in the brain: Motor syntax agents." Proceedings of the Eighth International Conference on Complex Systems NECSI: 1462-1476.
- Fraser, D. and J. C. Houk (2011). "Motor syntax disorder in schizophrenia." Proceedings of the Eighth International Conference on Complex Systems NECSI: 1516-1529.
- Ohta, H., Y. Nishida and J. C. Houk (2011). "Presynaptic inhibition and incremental learning in the striatum of the basal ganglia." Proceedings of the Eighth International Conference on Complex Systems NECSI: 1509-1515.
- Houk, J. C. (2011). "Can DPM brain agents write stories and sing songs?" Proceedings of the Eighth International Conference on Complex Systems NECSI: 1539-1548.
- Houk JC (2010). Voluntary Movement: Control, Learning and Memory. Encyclopedia of Behavioral Neuroscience. G. F. Koob, M. Le Moal and R. F. Thompson. Oxford, Academic Press. 3: 455-458.
- Botvinick M, Wang J, Cowan E, Roy S, Bastianen C, Patrick Mayo J, Houk JC (2009). An analysis of immediate serial recall performance in a macaque, , Animal Cognition 12:671-678
- Tunik E, Houk JC, Grafton ST. (2009). Basal Ganglia Contribution to the Initiation of Corrective Submovements.NeuroImage, 47: 1757-1766
- Wang J , Dam G, Yildirim S, Rand W, Wilensky U, Houk JC (2008). Reciprocity Between the Cerebellum and the Cerebral Cortex: Nonlinear Dynamics in Microscopic Modules for Generating Voluntary Motor Commands.Complexity 14(2): 29-45.
- Houk JC, Bastianen C, Fansler D, Fishbach A, Fraser D, Reber PJ, Roy SA, Simo LS (2007). Action selection in subcortical loops through the basal ganglia and cerebellum. Phil. Trans. R. Soc. B 362: 1573-1583.
- Houk JC (2007) Models of Basal Ganglia. Scholarpedia, 2(10):1633
- Houk JC (2007) Biological Implementation of the Temporal Difference Algorithm for Reinforcement Learning: Theoretical Comment on O’Reilly et al. Behavioral Neuroscience Vol. 121, No. 1, 231–232.
- Fishbach A, Roy SA, Bastianen C, Miller LE, Houk JC. (2007) Deciding when and how to correct a movement: discrete submovements as a decision making process. Exp. Brain Res.177:45-63
- Houk JC. (2005) Agents of the Mind. Biol. Cybern. 92: 427-437.
- Holdefer RN, Miller LE, Houk JC. (2005) Movement-Related Discharge in the Cerebellar Nuclei Persists After Local Injections of GABAA Antagonists. J. Neurophysiol 93:35-43.
- Fraser D, Park S, Clark G, Yohanna D, Houk JC. (2004) Spatial serial order processing in schizophrenia. Schizophrenia Research. 70:203-213.
- Houk JC, Mugnaini E. (2003) Cerebellum. In Larry Squire's Fundamental Neuroscience, V. Motor Systems, Chapter 32. Elsevier Science, pp.1-46.
- Novak KE, Miller LE, Houk JC. (2002) The use of overlapping submovements in the control of rapid hand movements. Exp Brain Res 144:351–364.
- Houk JC, Miller LE. (2001) Cerebellum: Movement Regulation and Cognitive Functions. In: Encyclopedia of Life Sciences.
- James C. Houk, Andrew H. Fagg, Andrew G. Barto (2000) Fractional Power Damping Model of Joint Motion.
- Sherwin E. Hua, James C. Houk, Ferdinando A. Mussa-Ivaldi (1999) Emergence of symmetric, modular, and reciprocal connections in recurrent networks with Hebbian learning. Biol. Cybern. 81, 211-225
- Beiser DG, Houk JC. (1998) Model of cortical-basal ganglionic processing: encoding the serial order of sensory events. J Neurophysiol 79:3168-3188.
- Hua SE, Houk JC. (1997) Cerebellar guidance of premotor network development and sensorimotor learning.Learn.Mem. 4: 63-76.
- Houk JC, Buckingham JT, Barto AG. (1996) Models of the cerebellum and motor learning. Behavioral and Brain Sciences 19, 368-383
- Houk JC, Alford S (1996) Computational Significance of the Cellular Mechanisms for Synaptic Plasticity in Purkinje Cells. In: Behavioral and Brain Sciences. 19(3): 457-461.
- Houk, JC, Adams, JL, Barto, AG. (1995) A Model of How the Basal Ganglia Generate and Use Neural Signals that Predict Reinforcement. In Models of Information Processing in the Basal Ganglia. JC Houk, JL Davis, DG Beiser, eds., The MIT Press, pp. 249-270.
- Houk JC, Wise SP. (1995) Distributed modular architecture linking basal ganglia, cerebellum and cerebral cortex: Its role in Planning and controlling action. Cerebral Cortex 5: 95-110.
- James C. Houk, Joyce Keifer and Andrew G. Barto (1993) Distributed motor commands in the limb premotor network. Trends in Neurosciences Vol. 16: pp27-33.
- Houk JC (1988) Control strategies in physiological systems. FJ Reviews 97-111.
- Houk JC, Rymer, WZ (1981) Neural Control of Muscle Length and Tension. Handbook of Physiology--The Nervous System II. V.B. Brooks. Bethesda, MD, Am. Physiol. Soc.: 257-323.
- Houk JC (1979) Regulation of Stiffness by Skeletomotor Reflexes. Annual Reviews Journal. 99- 114.
- Houk JC (1978) Participation of Reflex Mechanisms and Reaction Time Processes in the Compensatory Adjustments to Mechanical Disturbances. Cerebral Motor Control in Man: Long Loop Mechanisms, Prog.clin. neurophysiol, vol 4. 193-215.
Investigating the neuronal circuits that underlie the functions of the hippocampus.
Our laboratory investigates the neuronal circuits that underlie the functions of the hippocampus, which is a region of the brain involved in learning and memory.
In particular, we are interested in the roles played by specific cell types such as GABAergic interneurons and Cajal-Retzius cells in regulating network synchronization, synaptic plasticity, and in guiding the correct development of the hippocampal structural and functional architecture.
Our goal is to discover novel synaptic mechanisms that are of physiological relevance, but may also provide original insights for the pathogenesis of neurological diseases such as epilepsy and neurodevelopmental disorders, which often target the hippocampus.
We take advantage of an integrated approach combining several techniques such as paired recordings from anatomically identified neurons, optogenetic, immunohistochemistry, light and electron microscopy applied to wild-type and transgenic animals.
For publication information and more, see J Gianmaria Maccaferri, MD/PhD, faculty profile.
Researching mechanisms of neuronal excitability and organization of brain microcircuits.
The lab has two main research lines: mechanisms of neuronal excitability and organization of brain microcircuits.
We pursue these two wide basic science interests by investigating scientific questions with immediate potential for bench to bed translation. In particular, altered neuronal excitability is involved in important pathologies such as epilepsy, neurodegenerative diseases and neuropathic pain. Similarly, understanding the local brainstem networks that underlie the generation and regulation of breathing is a necessary step to understanding the mechanisms of SIDS (Sudden Infant Death Syndrome). Finally, we are interested in the identification of the role of unipolar brush cells, a recently discovered cell type of the cerebellar cortex, in cerebellar microcircuits.
To investigate these questions we use multiple techniques such as electrophysiological recordings from neurons and dendrites in brain slices and cultures, PCR analysis of gene expression, histochemical analysis of protein expression and optogenetic manipulations.
For publication information and more, see Marco Martina, MD/PhD, faculty profile.
Understanding the nature of the somatosensory and motor signals within the brain that are used to control arm movements.
The primary goal of the research in my lab is to understand the nature of the somatosensory and motor signals within the brain that are used to control arm movements. Most of the experiments in my laboratory rely on multi-electrode arrays that are surgically implanted in the brains of monkeys. These “neural interfaces” allow us to record simultaneously from roughly 100 individual neurons in the somatosensory and motor cortices and thereby study the brain’s own control signals as the monkey makes reaching and grasping movements. We can also pass tiny electrical currents through the electrodes to manipulate the natural neural activity and study their effect on neural activity and the monkey’s behavior.
Current projects seek to understand:
- How motor cortical activity leads to the complex patterns of muscle contractions needed to produce movement
- How movement of the limb and forces exerted by the hand are “encoded” in the activity of neurons in the somatosensory cortex
We also study how these relations are affected by behavioral context: the magnitude and dynamics of exerted forces, the varied requirements for sensory discrimination, and the quality of the visual feedback that is provided to the monkey to guide its movements.
Along with this basic research, we can use these neural interfaces to bypass the peripheral nervous system, in order to connect the monkey’s brain directly to the outside world. We are developing neural interfaces that ultimately will use signals recorded from the brain to allow patients who have lost a limb to operate a prosthetic limb. The interface may also be used to bypass a patient’s injured spinal cord in order to restore voluntary control of their paralyzed muscles. Conversely, electrical stimulation of the brain will restore the sense of touch and limb movement to patients with limb amputation or spinal cord injury. This highly interdisciplinary work is enabled by numerous collaborations at Northwestern University and other institutions.
Investigating the sensory-motor system through a close interaction with artificial systems.
Our laboratory (the Robotics Lab at RIC) investigates the sensory-motor system through a close interaction with artificial systems. Specifically, we are interested in determining how the brain acquires, organizes and executes motor behaviors. We use robotic and interface technologies to investigate how humans adapt to radical changes in the environment and in body mechanics.
Consistent evidence indicates that the nervous system is capable of coping with changes in the body and in the environment by developing internal representations of the relationship between movement commands and their sensory consequences. In this sense, motor learning is not only about improving performance. Motor learning is a means by which our brain develops an understanding of the physical and statistical properties of the world. We are studying the basic properties of this learning process and how it may be exploited to facilitate rehabilitation. Other studies within our group are directed at facilitating bidirectional communications between the human body and artificial instruments, such as wheelchairs and computers. We wish to combine the biological mechanisms of learning with machine learning algorithms for reducing the burden that disabled people must currently endure for the efficient operation of systems such as powered wheelchairs and other assistive devices. In a nutshell: we want to create systems that learn and adapt to their users.
Understanding how the brain controls motor behavior is of clinical interest since alterations in neuromotor control due to stroke and other neurological impairments can severely limit motor function. Through our research we wish to create knowledge that can help restore motor functions in individuals with neurological disorders.
For publication information see PubMed.
Contact Dr. Mussa-Ivaldi at 312-238-1230 or the Robotics Lab at 312-238-1232
Research Assistant Professor
Studying the molecular and cellular mechanisms that control the formation and modification of dendritic spines in the mammalian brain.
Research in my laboratory centers on the molecular and cellular mechanisms that control the formation and modification of dendritic spines in the mammalian brain. These mechanisms underlie the normal development and plasticity of the brain, and contribute to higher brain functions, including cognitive, social, and communication behavior. However, when these mechanisms go awry, they lead to mental and neurological disorders. Our analysis integrates multiple organizational levels, from molecular, cellular, circuit, and rodent models, to human subjects. We employ both a “translational” strategy, utilizing basic mechanistic data we generate to understand disease pathogenesis, and a “reverse-translational” strategy, in which genetic, neuropathological, and imaging studies in human subjects help guide the discovery of novel mechanistic insight. The ultimate goal of these studies is to develop therapeutic approaches to prevent or reverse neuropsychiatric disorders, by targeting mechanisms that control dendritic spines and synapses.
Projects within Our Lab
- Mechanistic studies on the molecular mechanisms of dendritic spine plasticity. This line of research aims to identify and elucidate functions of novel molecular regulators of synaptic circuit modification during the lifespan. We investigate the formation, remodeling, and elimination of spiny synapses in neurons using both in vitro and in vivo models. We are particularly interested in signaling, adhesion, and scaffolding molecules that control cell-to-cell communication and mediate intracellular signaling by neurotransmitter receptors. My laboratory continues to investigate small GTPase pathways and the roles of guanine-nucleotide exchange factors, such as kalirin and Epac2, and their downstream targets Rac, PAK, Rap and Ras. In addition, we have made important contributions to understanding how synaptic activity controls synapse size and strength through a pathway involving NMDA receptors, CaMKII, kalirin, Rac1 and actin, how rapid synaptic plasticity in the brain is regulated by locally synthesized estrogen, how adhesion molecules including N-cadherin control synapse size and strength, and how dopamine and neuroligin control synapse stability though Epac2 and Rap1.
- Translational and reverse-translational studies on the molecular substrates of dendritic spine pathology. Investigations of genetic, neuropathological, and neuromorphological alterations in human subjects with psychiatric disorders have started to reveal the pathogenic mechanisms behind these illnesses, and are also guiding the discovery of unexpected basic mechanisms of brain development and function. Through studies performed in the lab and through collaborations, we investigate molecular and cellular alterations occurring in patients with schizophrenia, bipolar disorder, autism, and Alzheimer’s disease. We then use model systems, such as neuronal cultures or mice, to elucidate the functions and pathogenic mechanisms of key molecules. We are currently investigating the basic synaptic functions of several leading mental disorder risk genes, to understand how they contribute to normal brain function and to synapse pathology. Conversely, many molecules we have been studying in the lab have more recently been implicated in the pathogenesis of mental disorders through independent neuropathological or genetic studies. We have shown that molecules that control basic synapse structural plasticity, such as kalirin and Epac2, functionally interact with leading mental disorder risk molecules, such as neuregulin1, ErbB4, DISC1, 5HT2A receptors, dopamine receptors, neuroligin, and Shank3. We have generated mutant mice in which kalirin or Epac2 are ablated, and have shown that these molecules control behaviors relevant for mental disorders, such as sociability, working memory, sensory motor gating, and vocalizations. These animal models can thus help to understand the synaptic substrates of specific aspects of mental disorders. To investigate the abnormal regulation of these molecular pathways in schizophrenia, autism, Alzheimer’s disease, and the impact of these molecular abnormalities on disease phenotypes in human subjects, we are collaborating with neuropathologists, brain imaging experts, and geneticists who investigate human subjects.
Potential Clinical Implications of Our Work
Therapeutic reversal of neuropsychiatric disease by targeting synaptic connectivity. By harnessing the knowledge from our basic and reverse-translational studies, my goal is to develop novel therapeutic approaches to prevent, delay, or reverse the course of mental and neurodegenerative disorders. Because abnormal synaptic connections play central roles in the pathogenesis of schizophrenia, autism, and Alzheimer’s disease, pharmacological targeting of key molecules implicated in synaptic plasticity and pathology can rescue disease associated abnormalities, and thereby influence the outcome of the disease. We are currently developing transgenic animal models to validate synaptic signaling molecules as therapeutic targets in mental disorders. We are also developing cellular assays which we will use in high-throughput screens for small-molecule regulators of synapse remodeling. Our goal is to identify small-molecule regulators of synapse remodeling which can be taken into clinical trials as therapeutics aimed at reversing synaptic deficits, and thus cognitive dysfunction, in mental disorders.
In our studies, we employ a multidisciplinary approach, using an array of methods that include advanced cellular and in vivo microscopy, biochemistry, electrophysiology, manipulations of gene expression in vivo, mouse behavioral analysis, circuit mapping, and human genetics and neuropathology.
Contact the Penzes Lab via email.
Dolores Martin de Saavedra
Blanca Diaz Castro
Ruoqui Gao – MD/PhD Student
Katherine Blizinsky (joint with Dr. Lei Wang)
Jessica Fawcett Patel
Applying multiple tools of quantitative synaptic circuit analysis to elucidate the functional ‘wiring diagrams’ of neocortical neurons in the mouse motor cortex
Synaptic circuits in motor areas of neocortex engage in neural operations underlying many aspects of cognition and behavior – motor control, executive functions, working memory, and more – yet circuit organization at the synaptic, cellular, and molecular levels remains poorly understood in agranular cortex. What is the functional organization of these synaptic pathways? What cellular and circuit-level operations do neurons in these perform? How do these local circuits communicate with each other and how do they interact with subcortical systems in the basal ganglia and thalamus? The focus of our laboratory is to apply multiple tools of quantitative synaptic circuit analysis to elucidate the functional ‘wiring diagrams’ of neocortical neurons in motor cortex. We use laser scanning photostimulation (LSPS) microscopy, based on glutamate uncaging and channelrhodopsin-2 excitation, for rapid functional mapping of synaptic pathways onto single neurons in brain slices of motor cortex. We are also applying a variety of circuit analysis tools in efforts to identify circuit-level mechanisms in mouse models of disease, including autism, Rett syndrome, epilepsy, and motor neuron diseases.
View publications on PubMed.
For lab information and more, see Dr. Shepherd’s faculty profile.
Contact the Shepherd Lab at 312-503-0753.
Understanding the computational implications of neural dynamics.
The goal of our research is to understand information processing in the brain. We use mathematical models based on specific hypothesis about encoding and decoding aspects of neural activity, and use analytical and numerical techniques to investigate the implications of these hypothesis so that they can be validated, modified, or discarded as dictated by experimental data.
Our purpose is to understand the computational implications of neural dynamics. Our work relies on conceptual frameworks and mathematical tools from statistical physics, information theory, nonlinear dynamics, probability theory, and machine learning, and aims at formulating data driven models that illuminate specific aspects of information processing by networks of neurons.
Specific topics of interest include input-output characteristics of single cell and network models, encoding and decoding of information through neural activity, early stages of sensory processing, and the neural control of movement. We work in close collaboration with experimental groups, both at Northwestern University and at other institutions. Recently, we have focused on the interplay between neural connectivity, network dynamics, and computation, and on brain-machine interfaces for the decoding of neural activity in motor cortex and the encoding of sensory information via stimulation of somatosensory cortex. Our work on brain-machine interfaces is funded by NINDS, the National Institute of Neurological Disorders and Strokes within the NIH.
For lab information and more, see Dr. Solla’s faculty profile.
Contact the Solla Lab at 312-503-1408 or visit us on campus in the Montgomery Ward Building at 303 E. Chicago Avenue, Chicago, IL.
Understanding the principles of neuronal dysfunction in disease states
Our group has five research topics. The first topic area is what drives Parkinson’s disease (PD). Using a combination of optical, electrophysiological and molecular approaches, we are examining the factors governing neurodegeneration in PD and its network consequences, primarily in the striatum. This work has led to a Phase III neuroprotection clinical trial for early stage PD and a drug development program targeting a sub-class of calcium channels. The second topic area is network dysfunction in Huntington’s disease (HD). Using the same set of approaches, we are exploring striatal and pallidal dysfunction in genetic models of HD, again with the aim of identifying novel drug targets. The third topic area is striatal dysfunction in schizophrenia, with a particular interest in striatal adaptations to neuroleptic treatment. The fourth topic area is post-traumatic stress disorder and the role played by neurons in the locus ceruleus in its manifestations. The last topic area is chronic pain states and the impact these have on the circuitry of the ventral striatum.
Visit the following external websites, organized by principal investigators, for details on the labs’ faculty, publications, past and current studies, and more.
Mussa-Ivaldi Lab (Robotics Lab)